房室折返性心动过速的心电图诊断

房室折返性心动过速的发生率约占室上性心动过速的50%。是房室之间存在异常传导通路—旁路引发。窦性心律时,激动经房室结和旁路同时下传激动心室,形成室性融合波,体表心电图出现预激综合征特有的心电图改变:①PR间期<0.12s;②QRS波增宽>10s;③有δ波;④继发性ST-T改变;⑤不合并束支阻滞时,QT间期正常。隐匿性旁路只有逆传功能而无前传功能,激动只能经房室结前传,旁路逆传。表现为窦性心律时体表心电图正常,心动过速发作符合房室折返性心动过速的特征。一、房室折返性心动过速的种类与机制房室折返性心动过速可分成:①顺向型房室折返性…     

特殊的1:2房室传导(综述)

1:2房室传导是指1个房性激动同时通过2个传导性及不应性不等的途径下传至心室,并引起2次心室激动。心电图表现为1个P波后继2个QRS波,易误诊为结性或室性早搏、心动过速等,通常需赖电生理检查方能确诊。本征根据传导途径可分2种:1种为1个房性激动通过房室旁道,同时还通过正常结希区,二者先后激动心室。另一种为1个房性激动同时通过房室结快慢径路先后下传到心室。兹介绍于下。     

食管心脏电生理技术与临床应用（4）--食管心脏电生理技术基础

1食管心脏电生理检查的基本参数 1.1心脏起搏术语（1）S波：为刺激仪发放的电脉冲形成,在心电图上表现出高尖的钉状波。（2）起搏P波：有效起搏后的心房激动波,与S波密切相关,如S波后无P波表示该次电脉冲起搏无效（心房处于有效不应期时例外）。（3）起搏QRS波群：心房起搏激动沿房室结-希浦系统或房室旁道顺传形成的心室激动波,形态应与窦性激动一致。形态异常时,要根据电生理特性进行分析,注意房室传导关系和QRS形态。（4）S1引起的P波、QRS波群称为P1、R1,S2引起的P波、QRS波群称为P2、R2。余分别以此类推。（5）S-P间期：从S波起始到P波起始,代表电脉冲经食管至心房开始激动时的时距。（6）S-R间期：从S波起始到QRS波群起始,在S波有效起搏心房,但其后P波不清楚时代表房室传导时间。（7） P1-R1（S1-R1）间期：代表基础刺激时的房室传导时间。（8）P2-R2（S2-R2）间期：代表S2期前刺激时的房室传导时间。（9）逆行P波：在房室折返性心动过速、房室结折返性心动过速、室性心动过速、房室交接区性期前收缩、室性期前收缩等发生逆传时形成的P波,以P-波表示。（10）逆行心房激动顺序：①中心性激动：心律失常时激动沿房室结或间隔部房室旁道逆传至心房,造成间隔部心房肌先激动,然后分别向两侧心房传导,这种左、右心房几乎同时开始激动的顺序称为中心性激动。心电图表现出V1与食管导联的P-波几乎同时出现;②右侧偏心性激动：房室折返性心动过速时激动沿右侧壁房室旁道逆传至右心房,然后通过房间隔向左心房传播,这种逆传心房激动顺序称为右侧偏心性激动,心电图表现出V1的P-波早于食管导联出现;③左侧偏心性激动：房室折返性心动过速时激动沿左侧壁房室旁道逆传至左心房,然后通过房间隔?     

房室结双径路折返性与非折返性心动过速一例

1例女性,65岁的患者,发作性心悸5年。发作时体表心电图提示窄QRS心动过速,约190次/分,P波与QRS波呈1∶2关系,RR间期长短交替现象。经心内电生理检查证实为房室结非折返性心动过速,术中也可诱发房室结折返性心动过速,经改良房室结慢径后获得成功治疗。     

房室结折返性心动过速伴房室阻滞的心脏电生理特点

目的利用食管法心脏电生理检查探讨房室结折返性心动过速伴房室阻滞的电生理特点。方法回顾分析经食管法电生理检查中房室结折返性心动过速伴房室阻滞18例患者的资料。结果房室结折返性心动过速伴房室阻滞主要表现为2:1房室阻滞,多在诱发开始时出现数秒至数分钟,也可呈持久性存在,2:1传导转为1:1传导时多经过一过性3:2文氏传导并伴一过性束支阻滞。结论P波极向及P波与QRS波群的关系特点是房室结折返性心动过速伴2:1房室阻滞的诊断依据。以此排除房室折返性心动过速,并注意与房速相鉴别。     

快慢型房室结折返性心动过速的电生理特点

目的观察快慢型房室结折返性心动过速的体表心电图和心内电生理特点.方法分析29例快慢型房室结折返性心动过速(FS,简称FS组)的体表心电图和心内电生理参数,并与61例慢快型房室结折返性心动过速(SF,简称SF组)的心内电生理进行比较.结果FS组心电图RP＞PR,PR间期平均为122±37 ms,其中5例PR≤100 ms,P波在QRS波群之前,类似交界区心动过速,P波在Ⅱ、Ⅲ、aVF导联为完全负向,V1导联为负正双向.FS组无AH间期跳跃现象较SF组更常见(69.0%vs.19.7%,有显著性差异P＜0.05);FS组心房和心室刺激更易诱发心动过速(79.3%vs.6.6%,有显著性差异P＜0.05).结论FS具有独特的体表心电图和心内电生理特点,这些特点有助于其诊断和射频导管消融治疗.     

差异性传导对房室及房室结折返性心动过速心内电图的影响

目的 分析差异性传导对室上性心动过速心内电图产生影响的机制,探讨解决问题的方法。方法 选择室上性心动过速病人357例,其中房室折返性心动过速出现差异性传导26/187例,房室结折返性心动过速出现差异性传导6/170例,观察出现差异性传导时心内电图的影响。结果 房室结折返性心动过速出现差异性传导时,心动过速的频率和心内电图无改变。右侧旁道介导的房室折返性心动过速出现右束支差传导心电图类似于慢一快型房室结折返性心动过速,同时伴心率下降。出现左束支差传时,心电图类似于慢一慢型房室结折返性心运过速或房速,心率不变,左侧旁道介导的房室折返性心动过速出现差传时,心内激动顺序不变,出现左束支差传时心率下降,右束支差传时心率不变。结果 差异性传导对房室结折返性心动过速及左侧旁道介导的房室折返性心动过速心内电图无影响。但对右侧旁道介导的房室折返性心动过速心内电图有较大的影响,旁道的电生理特性结合电生理检查有助于鉴别诊断。     

房室结折返性心动过速合并房室结-希浦系统传导阻滞

房室结折返性心动过速（AVNRT）是阵发性室上性心动过速的常见类型,也是房室结双径路传导在体表心电图的表现形式之一。QRS波群与P^-波的关系直接反映了AVNRT的形成机制,也是体表心电图分析及诊断的主要依据。但P^-波常被QRS波群掩盖,给诊断带来一定的困难。除了诱发及终止AVNRT时的心电图表现对诊断有帮助外,AVNRT出现房室结或希一浦系统传导阻滞时的电生理及心电图改变对其诊断与鉴别诊断也有极大的帮助。     

经食管心脏电生理检查误诊房室折返性心动过速的不典型房室结折返性心动过速的特点及分析

目的探讨食管电生理检查中被误诊为房室折返性心动过速的不典型的慢快型房室结折返性心动过速的特点。方法回顾性分析5例误诊为房室折返性心动过速患者的食管电生理及心内电生理资料。结果 5例患者在食管电生理检查S1S2程控期前刺激中,均未观察到S2-R间期有跳跃性延长,心动过速的R-P-EB间期70ms;逆行P-波在V1导联直立,下壁导联倒置;食管电生理诊断为左后间隔隐匿性旁道参与的房室折返性心动过速。心内电生理诊断为慢快型房室结折返性心动过速,并成功消融慢径路。结论部分R-P-EB间期70ms的不典型慢快型房室结折返性心动过速食管电生理特点与后间隔隐匿性旁道参与的房室折返性心动过速类似,必要时需心内电生理检查加以明确。     

不典型房室结折返性心动过速并左侧旁观者旁道一例

患者男性,48岁.因反复发作性心悸行电生理检查,心动过速发作时腔内A波激动顺序呈现由"偏心"转为"向心"的动态变化,变化过程中心动过速周长恒定,且希氏束电极上VA间期、HA间期及体表Q RS波形态均恒定不变,提示存在左侧旁道,且旁路传导与否并未影响折返环.诊断为不典型房室结折返性心动过速合并左侧游离壁旁观者旁道,实施旁...     

Paradoxical responses to pacing maneuvers differentiating atrioventricular node reentrant tachycardia and junctional tachycardia

A 40-year-old female presented at our hospital because of heart palpitations. During an electrophysiological study, atrioventricular (AV) conduction showed dual AV nodal physiology. Three types of supraventricular tachycardia (SVT) were induced. The initiation of SVT was reproducibility dependent on a critical A–H interval prolongation. An early premature atrial contraction during SVT repeatedly advanced the immediate His potential with termination of the tachycardia, indicating AV node reentrant tachycardia (AVNRT). However, after atrial overdrive pacing during SVT without termination of the tachycardia, the first return electrogram resulted in an AHHA response, consistent with junctional tachycardia. The mechanism of paradoxical responses to pacing maneuvers differentiating AVNRT and junctional tachycardia was discussed.     

伴连续性房室结功能曲线的房室结折返性心动过速的电生理分析

目的：探讨无房室结双径路特性的房室结折返性心动过速(AVNRT)的电生理特点。方法：所有心动过速患射频消融前常规行心内电生理检查。结果：845例射频病人中325例为AVNRT，其中有21例患房室结功能曲线呈连续性，其电生理特征：希氏束图上心房回波(A)先出现，A波落在室波升支或其前，希氏柬不应期内刺激心室，不能提前夺获心房，射频消融后心房刺激时AHmax明显缩短。结论：伴连续性房室结功能曲线的AVNRT患心房刺激不表现房室结双径路的电生理特性，其消融终点初步定为：心房心室S1S1、S1S2刺激不诱发AVNRT；无AHvH传导曲线跳跃；房室结前传不应期明显缩短。     

A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory

OBJECTIVE: The purpose of this study was to determine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during paroxysmal supraventricular tachycardia is a useful diagnostic maneuver in the electrophysiology laboratory. BACKGROUND: Despite various maneuvers, it can be difficult to differentiate atrial tachycardia from other forms of paroxysmal supraventricular tachycardia. METHODS: The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction was studied during four types of tachycardia: 1) atrioventricular nodal reentry (n = 102), 2) orthodromic reciprocating tachycardia (n = 43), 3) atrial tachycardia (n = 19) and 4) atrial tachycardia simulated by demand atrial pacing in patients with inducible atrioventricular nodal reentry or orthodromic reciprocating tachycardia (n = 32). The electrogram sequence upon cessation of ventricular pacing was, categorized as "atrial-ventricular" (A-V) or "atrial-atrial-ventricular" (A-A-V). RESULTS: The A-V response was observed in all cases of atrioventricular nodal reentrant and orthodromic reciprocating tachycardia. In contrast, the A-A-V response was observed in all cases of atrial tachycardia and simulated atrial tachycardia, even in the presence of dual atrioventricular nodal pathways or a concealed accessory atrioventricular pathway. CONCLUSIONS: In conclusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction is highly sensitive and specific for the identification of atrial tachycardia in the electrophysiology laboratory.     

小儿室上性心动过速的食管心电生理分型及演变

目的 :探讨小儿室上性心动过速 (SVT)的类型及其电生理特征 ,以及食管起搏对小儿SVT的干预作用。方法 :对 4 7例 8个月～ 15岁有SVT发作史的患儿进行了食管心电生理研究。结果 :4 7例SVT经食管心房调搏 (TEAP)确定分型 4 2例 (89.4 % ) ,其中旁路折返 2 8例 (6 6 .7% ) ,房室结内折返 10例 (2 3.8% ) ,心房内折返l例 ,窦房结折返l例 ,心房自律性增高 2例 ;不能定型 5例 (10 .6 % )。结论 :小儿SVT近 95 %为折返机制所致 ,以旁路折返最常见 ,其次为房室结内折返 ,与成人报道不同 ,可能与小儿传导系统发育规律以及旁路电生理特性发生演变有关     

Comparative study of transesophageal atrial pacing and intracardiac electrophysiology in patients with supraventricular tachycardia

The diagnostic value of transesophageal atrial pacing in supraventricular tachycardia (SVT) has been discussed according to the comparison of the results of intracardiac and transesophageal electrophysiological study. Some quantitative criteria for the differential diagnosis of atrioventricular node reentrant tachycardia (RT-AVN) and atrioventricular reciprocating tachycardia (RT-AP) has been proposed. We found that RT-AVN and RT-AP could be separated by noninvasive transesophageal atrial pacing. We also suggested that induced SVT would be RT-AVN if (1) SR conductive curve was not continuous and SR jump greater than 70 ms, (2) AV interval less than 60 ms, and it would be RT-AP if (1) SR curve was continuous and there was no SR jump phenomenon, (2) VA interval greater than 100 ms. Thus, transesophageal atrial pacing was very helpful in distinguishing the mechanisms of SVT and could provide a simple clinical cardiac electrophysiological procedure in diagnosing SVTs.     

Paroxysmal atrial fibrillation with and without primary atrial vulnerability. Clinical and electrophysiological differences

Primary atrial vulnerability defined as induction of repetitive atrial firing by a single atrial extrastimulus cannot always be demonstrated in patients with paroxysmal atrial fibrillation. The authors studied the electrophysiological differences between paroxysmal atrial fibrillation with and without primary atrial vulnerability. In 14 of 31 patients with documented history of atrial fibrillation, single extrastimulation at the high right atrium initiated repetitive atrial firing defined as rapid disorganized atrial activity continuing longer than 1 second. In the 14 patients with vulnerable atrium, the atrial effective and functional refractory were periods significantly shorter and the duration of the local atrial electrogram of the premature beat was longer and was fractionated. The % sinus node recovery time was longer in patients without vulnerability. Nine of the 17 patients without atrial vulnerability had sinus node dysfunction, and 4 of the remaining 8 patients had a repetitive type of atrial automatic tachycardia. In contrast, only 3 (21%) of the 14 patients with vulnerability had sinus node dysfunction, and none showed repetitive atrial tachycardia. The high prevalence of sinus node dysfunction or repetitive type of atrial automatic tachycardia in patients without primary atrial vulnerability suggests that these transient electrophysiological modifications which are not dealt with in the basic conditions may have a role in the enhancement of atrial vulnerability.     

Paroxysmal nonreentrant supraventricular tachycardia due to simultaneous fast and slow pathway conduction in dual atrioventricular node pathways

Electrophysiologic studies were performed on a 49 year old woman who had paroxysmal nonreentrant supraventricular tachycardia due to simultaneous anterograde conduction through dual atrioventricular (AV) node pathways. Slow pathway conduction was inversely related to the preceding sinus cycle length and fast pathway conduction was determined by the Hs-A interval (measured from the His potential due to slow pathway conduction to the onset of the subsequent atrial electrogram). Major determinants of sustained simultaneous anterograde fast and slow pathway conduction during sinus rhythm were 1) a retrograde unidirectional block in both fast and slow pathways, and 2) a critical conduction delay in the slow pathway and a long enough Hs-A interval to allow sequential conduction of impulse from both pathways. Flecainide was successful in preventing recurrences of the tachycardia by eliminating slow pathway conduction during long-term follow-up.     

心脏房室瓣周房性心动过速的电生理特征及射频消融治疗

目的报道一组起源于房室瓣环或其邻近心房肌(瓣周)的房性心动过速(房速)。方法16例患者经心电生理检查及射频消融证实为瓣周房速,并对电生理机制、靶点图特征、分布区域等进行分析。结果瓣周房速占同期射频消融治疗房速的23.2%,起源点在左、右侧房室瓣环的分布比为3∶16;体表心电图特征、发生机制与其他房速相比,差异无统计学意义。消融成功靶点均有A、V两种成分,A、V电位幅度之比为2∶3~6∶1,靶点局部A波电位提前于体表心电图P′波20~46(38.6±6.7)ms;瓣环标测和消融成功率87.5%,复发率7.1%。结论瓣周房速在全部房速中占有相当比例,起源点分布右侧显著多于左侧。其电生理机制与其他房速无明显区别,瓣环标测和消融在房速射频消融中有较大的实用价值。     

Provocation of supraventricular tachycardias by an intravenous class I antiarrhythmic drug.

Antiarrhythmic drugs may aggravate or induce ventricular arrhythmia. The induction of a supraventricular tachycardia or its facilitation has rarely been reported. The purpose of the study was to know whether the potential for supraventricular proarrhythmic effect of a class Ia intravenous antiarrhythmic drug can be exposed during electrophysiologic study. Ajmaline was chosen because of its short duration of action. The protocol of the study consisted of an electrophysiological study and programmed atrial stimulation using 1 and 2 extrastimuli on driven rhythm and atrial pacing up to second-degree atrioventricular block. Then 1 mg/kg of ajmaline was injected and atrial pacing was performed 3 minutes after its injection. Supraventricular proarrhythmic effect of ajmaline was defined as the spontaneous occurrence of a supraventricular tachycardia or the facilitation of its induction. Seventy patients among 1955 presented a proarrhythmic effect: 63 developed a supraventricular tachyarrhythmia (atrial flutter, fibrillation, tachycardia) and 7 an atrioventricular reentrant tachycardia, either spontaneously (n = 23) or during atrial pacing (n = 47). Risk factors were identified in most patients: old age, underlying heart disease, history of spontaneous supraventricular tachycardia and/or induction of a supraventricular tachycardia by 2 extrastimuli on driven rhythm in the control state (34 patients), sinus node dysfunction (22 patients). Compared with patients without proarrhythmic supraventricular effect only the history of spontaneous supraventricular tachycardia and the existence of a sinus node dysfunction were significantly more frequent (P less than 0.05) in patients with proarrhythmic effect of ajmaline. In conclusion, the supraventricular proarrhythmic effect of intravenous ajmaline exists and is related both to the electrophysiologic characteristics of the drug and to the arrhythmia substrate. The results indicate that a supraventricular tachyarrhythmia may be induced by a class I antiarrhythmic drug.     

Complete abolition of the reentrant supraventricular tachycardia zone using a new modality of cardiac pacing with simultaneous atrioventricular stimulation

In an attempt to prevent recurrent reentrant supraventricular tachycardia, an experimentally designed new pacemaker has been developed. The pacemaker, when connected to both atrial and ventricular electrodes, is capable of sensing either an atrial or ventricular signal and, in turn, triggers simultaneous atrioventricular (A-V) stimulation. Efficacy of this pacemaker was tested in four patients with recurrent paroxysmal A-V nodal reentrant tachycardia during electrpphysiologic studies. After connection of the electrodes to the new pacemaker, all atrial or ventricular premature stimuli elicited simultaneous A-V stimulation with resultant impulse collision in the A-V junction. Consequently, the reentrant tachycardia zone was completely abolished in all patients. This study has thus demonstrated the clinical feasibility of simultaneous A-V pacing to abolish the supraventricular tachycardia zone in man.